THE RELATIONSHIP BETWEEN TRANSCRIPT EXPRESSION
LEVELS OF NUCLEAR ENCODED (TFAM, NRF1) AND
MITOCHONDRIAL ENCODED (MT-CO1) GENES IN SINGLE
HUMAN OOCYTES DURING OOCYTE MATURATION Ghaffari Novin M, Allahveisi A, Noruzinia M, Farhadifar F,
Yousefian E, Dehghani Fard A, Salimi M *Corresponding Author: Dr. Azra Allahveisi, Department of Anatomical Sciences, Faculty of Medicine, Kurdistan
University of Medical Sciences, Pasdaran Street, Sanandaj, Iran. Tel: +98-873-664-673. Fax: +98-873-364-
674. E-mail: allavaisie@gmail.com page: 39
|
INTRODUCTION
Oocyte maturation and oocyte quality are important
parameters in successful reproductive results
of the assisted reproduction technologies (ART).
Mitochondria are the most abundant organelles in
the cytoplasmic oocyte [1]. They are necessary for
adenosine triphosphate (ATP) generation through
oxidativephosphorylation (OXPHOS), unlike any
other process of the cell, and depend highly on the
expression of proteins encoded by the mitochondrial
and nuclear encoded gene [1,2]. Mitochondria are
inherited exclusively from the mother [3]. Indeed,
mitochondrial function is associated with mitochondrial
DNA (mtDNA) [4,5]. The mitochondrial genome
encodes essential proteins, which are crucial
for the generation of ATP. These proteins are transcribed and translated in the mitochondrial matrix
[6]. Human oocyte mitochondrion has only a single
copy of the genome, which is representative of the
mitochondrial number. However, it has been clearly
documented that mtDNA number is expanded during
oocyte growth [7].
Mitochondrial biogenesis is managed independently
from the nuclear genome and depend on
regulatory coordination between the nuclear and mitochondrial
genomes [8]. However, little is known
about the regulation of mitochondrial gene expression,
compared with nuclear genes [8]. Regulatory
coordination of the nuclear and mitochondrial genes
are important in cell survival and energy homeostasis
[9]. Two products of these genes, NRF1and
TFAM, are well-known essential ubiquitous factors
for the mtDNA replication and expression [10]. The
NRF1 gene contributes in regulating the expression
of nuclear encoded components of the mitochondrial
respiratory chain [11]. The human TFAM is a 25 kD
protein with nuclear-encoded high-mobility group
(HMG) box protein, which plays an important role
through sequence binding to the heavy strand promoter
(HSP) and light strand promoter (LSP) sites in
the D-loop of human mtDNA, a control region that
regulates mtDNA transcription and replication [12-
14]. The TFAM gene has various functions, including
packaging mtDNA into a nucleoid-like complex
and maintaining and repairing mtDNA molecules
[15,16]. NRF1 has also been shown to be linked to
the promoters of the TFAM gene [17]. Their important
roles have been demonstrated by transgenic experiments,
showing that depletion of mtDNA in TFAM
and NRF1 homozygous knockout mice resulted in
the animals’ deaths [18,19]. Another factor, MT-CO1,
is a terminal component and one of the three genes
of mitochondrial respiratory chain, encoded by the
mtDNA [19-21]. Transcription levels of the MT-CO1
gene may possibly be an indirect indicator of the
mtDNA metabolic activity.
Active transcription of the mitochondrial genome
has been demonstrated to initiate at various developmental
stages, depending on the species [22]. Reports
from many studies suggested that gene-specific transcription
factors directly affect gene transcription in
mitochondria [23]. However, relationship between
the expression levels of nuclear and mitochondrial
encoded genes during human oocyte maturation is not
well understood. The aim of the current study was to
quantify the relationship between relative expression
levels of NRF1 and TFAM, and the MT-CO1 genes in
single human oocytes at various stages of the human
oocyte maturation from germinal vesicle (GV) stage
to metaphase II (MII) stage.
|
|
|
|
|
Number 26 Number 26 VOL. 26(2), 2023 All in one |
Number 26 VOL. 26(2), 2023 |
Number 26 VOL. 26, 2023 Supplement |
Number 26 VOL. 26(1), 2023 |
Number 25 VOL. 25(2), 2022 |
Number 25 VOL. 25 (1), 2022 |
Number 24 VOL. 24(2), 2021 |
Number 24 VOL. 24(1), 2021 |
Number 23 VOL. 23(2), 2020 |
Number 22 VOL. 22(2), 2019 |
Number 22 VOL. 22(1), 2019 |
Number 22 VOL. 22, 2019 Supplement |
Number 21 VOL. 21(2), 2018 |
Number 21 VOL. 21 (1), 2018 |
Number 21 VOL. 21, 2018 Supplement |
Number 20 VOL. 20 (2), 2017 |
Number 20 VOL. 20 (1), 2017 |
Number 19 VOL. 19 (2), 2016 |
Number 19 VOL. 19 (1), 2016 |
Number 18 VOL. 18 (2), 2015 |
Number 18 VOL. 18 (1), 2015 |
Number 17 VOL. 17 (2), 2014 |
Number 17 VOL. 17 (1), 2014 |
Number 16 VOL. 16 (2), 2013 |
Number 16 VOL. 16 (1), 2013 |
Number 15 VOL. 15 (2), 2012 |
Number 15 VOL. 15, 2012 Supplement |
Number 15 Vol. 15 (1), 2012 |
Number 14 14 - Vol. 14 (2), 2011 |
Number 14 The 9th Balkan Congress of Medical Genetics |
Number 14 14 - Vol. 14 (1), 2011 |
Number 13 Vol. 13 (2), 2010 |
Number 13 Vol.13 (1), 2010 |
Number 12 Vol.12 (2), 2009 |
Number 12 Vol.12 (1), 2009 |
Number 11 Vol.11 (2),2008 |
Number 11 Vol.11 (1),2008 |
Number 10 Vol.10 (2), 2007 |
Number 10 10 (1),2007 |
Number 9 1&2, 2006 |
Number 9 3&4, 2006 |
Number 8 1&2, 2005 |
Number 8 3&4, 2004 |
Number 7 1&2, 2004 |
Number 6 3&4, 2003 |
Number 6 1&2, 2003 |
Number 5 3&4, 2002 |
Number 5 1&2, 2002 |
Number 4 Vol.3 (4), 2000 |
Number 4 Vol.2 (4), 1999 |
Number 4 Vol.1 (4), 1998 |
Number 4 3&4, 2001 |
Number 4 1&2, 2001 |
Number 3 Vol.3 (3), 2000 |
Number 3 Vol.2 (3), 1999 |
Number 3 Vol.1 (3), 1998 |
Number 2 Vol.3(2), 2000 |
Number 2 Vol.1 (2), 1998 |
Number 2 Vol.2 (2), 1999 |
Number 1 Vol.3 (1), 2000 |
Number 1 Vol.2 (1), 1999 |
Number 1 Vol.1 (1), 1998 |
|
|